CPAPtalk.com

Chuck, are you sure that you did every step the same? cpaptalk.com accepts only .jpg or .gif pictures. If you rightclick your previous picture in your post on page 11 of this thread and look at the very last word in the URL linking to Photobucket, your graph picture is a ".jpg", just like it should be.

Perhaps there's a step to take in Photobucket to convert the tiff you uploaded into a jpg. Then it can be linked to in a post in cpaptalk.

RG-

The file that Grab captures of the image is a TIFF file. I checked the file type for the chart that I successfully uploaded and it was, in fact, a TIFF file too. I just tried repeating the exact same procedure as I used the first time, and again, Photobucket refuses to upload a TIFF file (even though the first graph was a TIFF). I checked in Photobucket and there isn't a utility to convert a TIFF to a jpeg, best as I can see.

So, color me confused.

Chuck

With David's (DMW) kind and EXCELLENT help, here's the graph depicting the APAP/Swift trial (7/9-7/16) and the APAP/Activa trial (7/3-7/9). Next comes CPAP (8cmH2O)/Swift trial starting tonight.



Cheers!

Chuck

As strange luck would have it, I experienced a CSDB epiphany late last night. As highly improbable as it sounds, I think I just may have solved the riddle of why and how CO2 maladjustment occurs in the case of CSDB. And if I haven't solved the underlying CSDB riddle itself, then at least I have constructed a cohesively plausible CSDB theory, and that type of excercise in and of itself is never a bad endeavor in life IMHO.

As it turns out, I believe that there is an inferential relationship between c-fiber afferents and the peripheral chemoreceptors. And that inferential relationship is precisely what causes the CO2 inspiratory "target" itself to get set too high at times. It's also what causes that "counterproductive" CSDB defensive airway closure. I'll explain it all as we go along. Fellow CSDB sleuths, please stay tuned. This thread just got that much more interesting. .

Fascinating Steve!!! I'd love to hear your reasoining about this!!!

I just participated in a thread with another user who just switched from a Swift to an HC431 and finds a marked change in her level of consciousness, as I did after switching from the Swift to an Activa. I am intrigued about the issue of differentials in dead-space for those of us that may be sensitive to CO2 levels.

I'll enjoy seeing how this unfolds.............

Chuck

Topmost is the PSG chart showing CSDB central apneas:


The text excerpt for the two PSG charts above follows:

"Enhanced expiratory rebreathing space enhancement of positive airway pressure therapy. Above, severe central sleep apnea occurring on the application of positive airway pressure to a patient with complex disease. Both snapshots have 'dead space' added by use of a nonvented mask and additional tubing, and show a dose response that results in small increases in end-tidal CO2. With 50 ml dead space, end-tidal CO2 is 38 mm Hg, and central apneas continue; further increase of dead space to 150 ml results in an end-tidal CO2 of 43 mm Hg and complete control of disease. Biphasic positive airway pressure is 12/8 cm, spontaneous mode, throughout. Laboratory control is easier than home control, where mask leaks are inevitable. Even in the sleep laboratory, the precision of control in comparison with the PAPGAM is not possible because of leak, turbulence, and washout effects. This method does offer practical clinical benefits to patients who are otherwise unable to use positive airway pressure, and it validates the fundamental approach of hypocapnia minimization."

Once again, look at the nasal pressure, nasal flow, chest, and abdomen waveforms on the topmost PSG chart. When the nasal pressure and nasal flow data channels flatten out, so do the chest and abdomen data channels. If the chest and abdomen channels are flattened out then no central respiratory effort whatsoever is occurring. And those apneas get scored as central apneas versus obstructive.

So, CSDB is a complex sleep disordered breathing disease that typically starts off with obstructive apneas. Once positive pressure is applied, overt cases of CSDB will typically begin to manifest frank machine-induced central apneas---yet only during NREM or non-REM sleep. A very mysterious disorder, indeed: 1) it starts off pretty much exclusively obstructive, 2) the obstructive apneas can be amazingly cyclic and tend to be short, 3) once positive pressure is applied to correct the obstructive apneas, then central apneas appear, 4) yet those central apneas do not appear in REM sleep.

The fact that the CSDB central apneas do not occur in REM sleep got me to wondering. Was CSDB's central apnea absence in REM somehow related to the fact that our brain waves in REM sleep are remarkably like our brain waves during wakefulness? Was it because the dysregulating CSDB mechanism had emerged in the evolution of our sleep-induced autonomic breathing before REM ever had a chance to evolve? Or was it perhaps a combination of these two? Or perhaps neither?

And just as cryptic: why does CSDB manifest as a two-stage complex SDB condition? Why are there typically no hypocapnic central apneas before xPAP is applied? And why do the early-stage obstructive apneas often manifest with such clock-like periodicity? That extreme periodicity of the obstructive apneas themselves strongly hints at neurological dysregulation attributed to one or more chemoreceptor channels not being maintained. However, in physics that kind of periodicity might also be attributed to other factors including a natural rate of decay regarding musculature airway closure, arousal, then autonomic correction, followed by recurring musculature airway closure, etc. If that obstructive sequence occurred all by itself, then a highly improbable scenario of recurrent biomechanical energy decay might be considered.

However, since the highly periodic CSDB obstructive apneas occur in a disorder that always entails hypocapnic central apneas once positive pressure has been applied, then chemoreceptor-driven neurological disorder becomes the more likely case. And that still leaves us with the mystery as to why this neurologically dysregulated breathing condition is a two-phase phenomenon.

A trip through evolutionary history got me to once again wondering about autonomic breathing. Specifically I got to wondering about adaptive neural plasticity and its evolutionary roots... (to be continued)

I think when you see both obstructive and central events at the same time as in CSDB, CAN this mean something is possibly activating both a central and peripheral chemoreceptors response?. They are multiactivational.

What about the chemical aspect and CSF? doesn't a change in CSF pH make the medulla's response more or less sensitive?

Is it possible the external pressure from the PAP is activating one of these other chemoreceptor responses? Such as the Stretch receptor of the lungs?

My current lecture read says:
The most important factors affecting respiration are levels of oxygen, carbon dioxide and hydrogen ions in the plasma and cerebrospinal fluid. There are chemoreceptors dedicated to monitoring Po2, Pco2, and pH. Peripheral chemoreceptors are found primarily in the carotid sinuses and the aortic arch. Central chemoreceptors are found on the medulla oblongata. The peripheral chemoreceptors monitor plasma Pco2, pH, and Po2. Central chemoreceptors primarily monitor pH of cerebrospinal fluid.

Respiratory Control:
Let's see how both the central and peripheral chemoreceptors would respond to an increase in plasma CO2.

An increase in plasma Pco2 will directly and indirectly activate peripheral chemoreceptors. It'll directly activate those that are sensitive to Pco2. Recall the carbonic anhydrase equation and notice that an increase in Pco2 will yield an increase in plasma [H+], i.e., a decrease in pH. Thus an increase in Pco2 will be detected by plasma pH receptors due to the change in [H+]. An increase in plasma Pco2 will also cause CSF Pco2 to increase. Since CSF contains carbonic anhydrase, the increase in CSF Pco2 will cause a decrease in CSF pH. This will be detected by the medullary chemoreceptors. The net response to the high CO2 will be an increase in respiratory rate and depth.

(sorry dude, I'm totally lost without pictures ):


I was good at the knee bone connects to the chin bone...

I gotta toss this out there, in the top most PSG, chest and adomen activity cease during these events. If you had asthma for example, this could change how the streatch receptor responds. In this case I suspect the streatch receptor of the lung is the trigger due to inflation by the xpap machine of 12/8cm.

The xpap delivery pressure even though it is spontaneous mode is probably what is giving you your perfectly "timed" events. Change the xpap to the timed mode to a value we can see change

I have NOT started my CPAP trial. I did try once three evenings ago and found that I awakened in the middle of the night feeling poorly. The CPAP was set to deliver 8 cmH20. Since I was feeling so poorly, I reset the S8 to AutoSet and fell asleep soundly for the rest of the night. For the last two nights, I've continued with APAP and have slept relatively well (especially last evening when I got nearly 8 STRAIGHT hours). My 95% pressure has been running at 8.7 cmH2O on average and I've had AHIs of 3.0 on average. I'll try to work up the courage to return to a CPAP trial this weekend.

Chuck

P.S. Fascinating posts Steve. Thanks. I'll review them today.

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CPAPopedia Keywords Contained In This Post (Click For Definition): CPAP, APAP

Excellent diagrams, Snoredog! Thanks. You can see from that diagram what a primary role CO2 detection plays, and what a distant secondary role O2 detection plays. The human respiratory drive is largely CO2 driven regarding detection of blood gases. Great comments, too, Snoredog.

The major CSDB players or suspects so far: 1) the medulla and pons (neurologically controlling respiration---homeostatically, and sometimes even adaptively), 2) blood gas chemoreceptors, 3) afferent irritant receptors, 4) stretch receptors. Each of these chemoreceptor categories have pheno-subtypes discussed earlier and clearly outlined in Snoredog's diagrams.

In addition to the above suspects, CSDB also has a positional sequence of obstructive apneas while in the supine position being traded for central apneas while on either side. So add to that list of CSDB suspects positional sensors, specifically proprioceptors in the joints and muscles.

SWS wrote:

...specifically proprioceptors in the joints and muscles.

You mentioned the absence of CSDB during REM...

...during REM isn't the "muscle receptors" for the major limbs turned off or even deactivated?

For example, if you reached the wake state with the brain leaving these muscle groups off, you be experiencing the effects of what we think of sleep paralysis.

Just a thought... if the brain turns off those receptors during REM it could explain its absence.

This is interesting, more from lecture notes...

Other factors that can alter respiratory rates:

-Pain and emotions

-Irritating physical or chemical stimuli in the respiratory tract.

-Overstretch of the lungs - activates lung stretch receptors which act on brainstem centers to cause exhalation and prevent inhalation (this is known as the Hering-Breur reflex).

-BP changes as detected by carotid and aortic arch baroreceptors. A decrease in BP can result in an increase in respiration rate/depth.

-Changes in plasma and CSF Pco2, Po2, and pH.

this paper says the central receptors are the most important receptors.

if the lung gets over-streatched possibly by the Xpap machine pressure....

APAP/Swift

AHI=3.7;AI=0.3;HI=3.4;Press. (95%)=8.4.

Slept well. DREAMING!!!!

Since this thread has delved into CSDB and the dead-space titrations Harvard researchers have employed to correct hypocapnic central apneas (by compensating CO2 kinetic transitions with that additional dead space), I wanted to place a link to another thread about the AutoSet CS2. That AutoSet CS2 is a relatively new machine design that treats CSDB as well as other central apnea sub-phenotypes. It utilizes adaptive servo ventilation (instead of passive dead space techniques) to achieve adequate control over CO2 kinetic respiratory transitions:

viewtopic.php?t=11458&start=0
(please note the above ASV implementation has also been experimentally used in conjunction with dead space by some researchers for yet extended CO2 kinetic control)

Snoredog wrote:...during REM isn't the "muscle receptors" for the major limbs turned off or even deactivated?

The proprioreceptors are essentially positional sensors. Sleep position changes occur in NREM rather than REM. Once the proprioceptors neurologically convey an NREM positional change, that information is thought to be neurally stored. So then a relevant proprioreceptor question emerges: Where is this positional information neurologically stored and is it available for adaptive purposes of autonomic breathing's neural plasticity?

Snoredog wrote:..this paper says the central receptors are the most important receptors.

Presently, that is generally thought to be true, Snoredog. However, since CSDB patients generally do not completely or adequately respond to central-apnea-addressing pharmaceuticals that simply change CSF PH levels, we might assume that other chemoreceptor signals drive this disorder. Especially in light of the fact that this is a two-stage respiratory sleep disorder that most often starts the night without central apneas. I never did get around to placing stretch receptors in the discard pile, BTW.

More on this later.

-SWS wrote:DSM, thanks so very much for pointing out the impeller diagrams and making your comments. The impeller blades sit on opposite ends of the shaft toward a sole adaptive-servo objective of achieving tuned inertia. There is thus no directionally opposed impeller for the purpose of actively facilitating CO2 exhaust. That implicitly means that the AutoSet CS2 relies more on matching incrementally precise ventilatory pressures (exceptionally synchronized with respiration) to prevent CO2-based homeostatic maladjustment in the first place, than does it rely on having to compensate CO2 kinetics after inspiratory-trigger homeostatic-maladjustment has already occurred.

Or to simply summarize by comparing how the dead space and ASV techniques differ in addressing hypocapnic central apneas:

1) Additional Dead Space: does nothing to prevent CO2-based inspiratory-threshold maladjustment, but elevates CO2 kinetic retention to compensate for an already maladjusted CO2 inspiratory-trigger threshold.

2) Adaptive-Servo Ventilation: prevents CO2-based inspiratory-threshold maladjustment by avoiding typical xPAP ventilatory "overshoot", thereby often obviating the need for post-maladjustment compensation of CO2 kinetics.

Some researchers have successfully combined the dead space and ASV techniques to achieve yet additional hypocapnic based central apnea efficacy. These two techniques are not at all mutually exclusive as their respective mediatory effects occur during different stages of the maladjusted hypocapnic respiratory process.

There are very big underlying implications regarding the inherent contrasts in these two alternate yet complementary treatment methods. I will be using the above conclusions in the Apnea -v- Hypopnea thread to support a theory of CSDB as a two-stage SDB condition occurring as the result of a maladaptive homeostatic c-fiber afferent inferential relationship. This is all rather neatly piecing together in my own mind. I can't thank you enough for the diagrams and your comments, DSM.

Here is a diagram that shows adaptive-servo ventilation's very precisely synchronized delivery of minute support pressures that nicely avoid xPAP transient pressure "overshoot" to avoid CO2 homeostatic maladjustment in the first place:



The above image is taken from the following medical study:
Am. J. Respir. Crit. Care Med., Volume 164, Number 4, August 2001, 614-619
Adaptive Pressure Support Servo-Ventilation:
A Novel Treatment for Cheyne-Stokes Respiration in Heart Failure
HELMUT TESCHLER, JENS DÖHRING, YOU-MING WANG, and MICHAEL BERTHON-JONES
http://ajrccm.atsjournals.org/cgi/conte ... /164/4/614

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CPAPopedia Keywords Contained In This Post (Click For Definition): Hypopnea

I hate to cross post, but I need to get the above information explicitly stated in this thread, where theoretical CSDB discussions will continue.

-SWS wrote:That AutoSet CS2 is a relatively new machine design that treats CSDB as well as other central apnea sub-phenotypes. It utilizes adaptive servo ventilation (instead of passive dead space techniques) to achieve adequate control over CO2 kinetic respiratory transitions

I intend to show that the AutoSet CS2 avoidance of ventilatory overshoot is not an issue of CO2 kinetics as previously thought, and that additional dead space is a genuine CO2 kinetic mediating factor after homeostatic maladjustment has already occurred. I also intend to show an unexpected relationship among several chemoreceptor types in the second dysregulated stage of CSDB.